Quercetin protects H9C2 cells against hypoxia injury through MAPK/ERK1/2 signal pathway

Objective To investigate the effect and mechanism of quercetin on H9C2 cells against hypoxia injury. Methods The contents of lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined in a hypoxia model of H9C2 cells. MTT assay was used to measure the optimal concentration of quercetin to H9C2 cells. Then the H9C2 cells were divided into control group (C), hypoxia group (H), SCH772984 group (S), quercetin group (Q), quercetin+hypoxia group (Q+H), and quercetin+SCH772984 group (Q+S). After the treatment of each group was completed, the contents of LDH, SOD and MDA were successively detected, and the expression levels of MAPK, ERK1/2 proteins and their phosphorylation were observed. Results H9C2 cells were dependent on hypoxia culture conditions for a certain period of time. After 24 h of hypoxia culture, significant hypoxic damaged were observed. LDH and MDA contents were increased significantly while that of SOD was decreased significantly (P < 0.05). The results of MTT assay showed quercetin at a concentration of 10-6 mol/L significantly promoted the proliferation of H9C2 cells (P < 0.05), reduced the contents of LDH and MDA in the H9C2 cell of the Q and S groups (P < 0.05), and significantly increased the content of SOD (P < 0.05). In addition, the concentration also increased the phosphorylation levels of p-MAPK and p-ERK1/2 in H9C2 cells. Conclusion Quercetin can effectively resist the damage of H9C2 cells caused by hypoxia, improve antioxidant capacity, remove harmful substances produced during hypoxia, and activate the MAPK/ERK1/2 signal pathway to play an anti-hypoxic effect